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Cardiac Pharm (Antiarrhythmics (Class III (Potassium channel blockers)…

- - - - Propafenone/phone IC
        
        slows conduction B-blocking effects (bronchospasm) atrial arrhythmias cardioversion afib. prevent SVT;
      - Flecanide/flakes IC
        
        long-term control of refractory ventricular arryhtmias.slowing conduction in tissues making threshold harder to achieve and prolong AP blocking potassium. cardioversion prevent SVT w/ lack of MI
      - atrial flutter/fib, refractory ventricular arrhythmias w/out structural heart disease; CYP issues for both.
      - P-glycoprotein
    - - Prolong repolarization ^ risk of arrhythmia 3rd line; IV cause hypotension from Na loss of tone;for *WPW bypass tractshas dog lupus*
    - - IV treat ischemia, shortens phase 3 2nd choice Vtach (broken heart sign bottom lit); (doesn't impact conduction so no junction) only impacts sodium channels moving shorten action potential and decrease refractory CNS toxicity (hat-altered mentaition and nystagmus);
  - - - V arrhythmias!!! All 4 classes; pre-excitation afib, and drug of choice vtach particularly in patients who had an MI. least pro-arrhythmic; crosses BBB bluish skin and hypothyroid situations; inhibit CYP-450, P-glycoprotein
    - - B-blocking block phase 3 AP, affecting AV node used for SVT (atrial and vent.) w/ patients who had MI or CAD; B-blocking;
    - - shorter half life 2nd line can't cross BBB; sulfa;
    - - -cardioversion, for AVRT and WPW bypass tracts
  - - - involved in ATP synthesis impact sodium pump activity or ATPases can interact with phospholipids can stabilize membranes' treat torsaides (slow SA and myo conduction) and digoxin poisoning;
    - - shortens phase III and AP (sodium channel blocker; improving O2 supply; A & V arrhythmia; add-on; 2ndary anginas
    - - cardioversion. break acute SVT slow Av node conduction.
  - - - Inpatient management, IV BB (esmolol/quick turnaround-not on the list, propranolol, metoprolol (tartrate-(lopressor) short acting BB and succinate(toprol XL)-long acting)) or CCB (diltiazem, verapamil)
        If patient in shock or with severe hypotension, pulmonary edema, or ongoing MI/ischemia, cardioversion may be indicated (if medication can't work heart not moving) Poor perfusion, not awake, not appropriate oxygen
        
        cardio version: no contraindications, can use flecanide, dofetalide, propafenone, (1a) and ibutilide (1c) for pharmacologic cardioversion
    - - rate control and coagulation; Beta blocker or CCB first line- slow down nodal contraction for BB contraindications w/ anticoagulation
        In MI/Ischemia: Beta blockers (metoprolol if stable, esmolol if unstable not used in COPD pt.), preffered over cal channel blockers (diltiazem preferred over verapamil). Symptoms but awake and moving
    - - BB, nondihydro CCB mono therapy in older, combination in younger; CAD-BB; HF BB+digoxin; need anticoagulation of dabigatran, rivaroxaban, apixaban
- - - - enhanced uric acid excretion treat gout; first pass metabolism
    - - BID
    - - good for diabetic nephopathy
  - - - treat Liver Impairment
    - - IV; more cough and sx
    - - lowest side effects
  - - - B1 selective, long term oral; given to stable a-fib and sinus tach; less bronchospasm
    - - nonselective cardiac w/ out bronchi spastic lipid soluble (brain) (propane to the brain-fatigue, sexual dysfunction, insomnia)
    - - B3 trigger NO release
  - - - gestational HTN; HTN EMS
    - - HTN/CHF
  - - - block renin bad for renal more sx
  - - - Furosemide
        
        Unpredictable furious child holding onto water, chlorine and peanuts; short half life' used in renal failure up dose
      - Torsemide (torsion last longer)
        
        longest half life; better than furosemide
      - Bumetanide
        
        more potent and Bioavailability “better than furosemide”
      - direct blockage of NA-K-2Cl transporter of loop of henge, most effective used for pulmonary edema,
    - - Hydrocholorothiazide
        
        older
      - Chlorthalidone
        
        longer half-life; double potency; okay to use until CrCL >10 for kidney
      - inhibit Na-cl cotransporter in early DCT; keep magnesium, treat; decreased peripheral resistance over time
      - decreasing calcium loss out of the kidney; efficacy loss w/ NSAIDS
      - hypokalemia, hyperureceemia, hypotension, hyponatremia, hypercalcemia;
    - - Spironolactone (Spyro the Dragon-purple) man boobs
        
        aldosterone antagonist prevents heart remodeling, HFrEF, cirrhosis, inhibit Na/K in late distal tube and collecting duct, cause gynecomastia and good for preventing cardiac remodeling
      - Triamterene
        
        eNAC inhibiting Na/K ATPase in collecting duct endothelial channels
      - avoid in anuria, renal dysfunction can't filter it; make hyperkalemia (muscle placidity)
    - - Mannitol
        
        keeps urinary flow, IV, ICP, acute renal toxicity
        
        add solutes that do not undergo reabsorption
    - - Acetazolamide
        
        treat Altitude sickness
        
        treat glaucoma
        
        sx: Alkalosis/cause renal stones
        
        bicarb excretion
        
        inhibition of proximal tubule carbonic anhydrase; causes alkalosis
  - - - Nifedipine (fetishes are short lived, nympho); coronary spasm help w/ angina; most common adverse effects
      - Amlodipine (dipping sauces)
        
        long half-life (dip for long time); vasospastic angina
    - - Verapamil
        
        both more for contractility; AV nodal slowing; prevent SVT, AVRT, WPW (similar narrow complexes); constipation
      - Diltiazem
        
        vascular and cardiac, used for a-fib; less fx; used for vasospastic anginaprevents angina and helps w/ coronary spasm and dilation of them
  - - - A1; refractory Add-on; sexual dysfunction ortho hypotension
  - - - second line HTN
    - - For Mother’s pregnancy prodrug, Multiple dosing
- - - - Prasugrel
        
        ACS; 2-4 hours
        
        angioedema, bleeding, headache, hyperlipidemia, hypertension
      - TicagreloR
        
        Reversible! taken w/ aspirin inhibit ADP to GP binding; 1-3 hours
        
        bleeding, dyspnea, headache, raise SCr
      - Clopidogrel
        
        3-5 days; PAD
        
        bleeding SJS
      - inhibit binding of ADP to P2Y12 inactive GP; more useful than aspirin; more frequent serious bleeding, stent, M, ACS, MI, stroke; no change in vasoconstriction
    - - inhibit thromboxane inhibiting Cox-1; irreversible inhibition; cerebral ischemia and MI
      - angioedema, bleeding, bronchospasm, GI disturbances, reye syndrome, SJ
    - - inhibit phosphodiasterase so vasodilator (pyramid,moles like sand ) increase cAMP; stroke prevention BOTH; used w/ aspirin*thromboxane; stroke not unstable angina*
      - bleeding, GI discomfort, rash
  - - - interact w/ antithrombin III accelerating it; shut down II and 10; pregnancy; PT; intrinsic; not renal disease; can cause HIT (thrombocytopenia against factor 4); osteoporosis
        
        LMWH
        
        smaller less monitoring, less HIT; worry about bioaccumulation in renal disease
    - - factor 10; antithrombin III; similar w/ less HIT, not for renal; no reversal
    - - inhibit site of free and clot-bound thrombin; in PCI, at risk for HIT, unstable angina w/ angioplasty
  - - - involves 2,7,9, 10 preventing prothrombin 7 from combining w/ 10. prevent stroke w/ fib, and prostethics
      - monitor meds, CYP, INR dosing w/ lag time and bridging 2 days to change, 1 week to stabilize
      - vitamin K reverses after 24 : worry about diet
  - - - direct thrombin inhibitor clotted and free; VTE tx and prevention
      - reversal w/ idarucizumab
    - - targets factor 10a, no reversal; IND: DCT tx and prevention, PE
    - - target factor 10a, shorter half life; IND: CAD PAD anticoagulation VTE
  - - - target plasminogen and breaks down thrombin; catheter and shunt; window of usefulness; angioedema
      - target bound plasminogen-alteplase;
  - - - against warfarin
    - - reverse heparin by positive charge binding and not allowing it to interact w/ antithrombin III
    - - reverse dabagatran
    - - inhibits plasminogen activation, more potent, counter regulatory
  - - - Simvastatin
      - Atorvastatin
        
        both have higher maximal LDL lowering used in high-intensity
      - Rosuvastatin
      - Pitavastatin
      - decrease LDL increase LDL receptor and stop it from being made. improve endothelial function, plaque stabilization, anti-inflammatory
      - Sx: liver failure, myopathy, (The loss of the cholesterol (necessary for cell membrane) and mevalonyl precursors (sarcolemma-plasma of skeletal muscle) can occasionally generate muscle issues may generate myopathy complaining of muscle pain or measuring creatinine) and teratogenic
    - - decreases hepatic production of TG, VLDL and Apo B indirect triggering of increased HDL levels decreased liver degradation; inhibits lipolysis in adipose tissue; reduce triglyceride increase HDL
      - NADH precursor
      - flushing, hyperuricemia, gout, hepatotoxicity, hyperglycemia
    - - PPAR (peroxisome (breakdown lipid organelles) proliferation activated receptors) increase lipoprotein lipase, reduce VLDL and peroxisome decrease triglyceride
      - GI disturbance, gallstone (cholesterol bile excretion ^ more sent out), no renal failure
    - - prevent bile acid resorption causes constipation and impairment of vitamins reabsorbed in ileum and defectated out. promote conservation of cholesterol to bile acids ^ LDL receptors.
      - GI side effects, impairment of fat soluble vitamins; steatorrhea
    - - block cholesterol transport on gut epithelial; decrease liver store
      - liver and gut issues
    - - Alirocumab
        
        similar
      - Evolocumab
      - increases LDL receptors on surface by inhibiting their degradation
      - for maxed on statins
      - via injections develop allergies; works very well
    - - inhibit VLDL and TG synthesis by competing and changing cell membrane features competing for enzyme spots. decreaseing TG
      - Think of them competing for enzyme spots as for arachidonic acid and inflammation
      - GI effects, fishy taste (from consumption of the fish oil pills), and possible bleeding risks for those on anticoagulation
- - - - L-arginine NO> ^cGMP, ^dephosphorylation of myosin light chain>vasodilation of smooth muscles
      - reflex tachycardia, requiring intervals. ; postural hypotension, tolerance
    - - venodilation (storing fluid in veins) and headache, flushing, tachycardia, postural hypotension venodilator; longer half life
    - - dilates arterioles only not coronary potassium hyperpolarization inhibiting calcium release and stimulation of NO ; angina stimulates RAAS
      - headache, reflex tachycardia, palpitations, angina, nausea; taken w/ B blockers and diuretics
- - - - enhance vagal tone SLOWER AV NODE conduction by ^intracellular Ca and decreasing Ca exchanger out of cell inhibit potassium side of pump; 3rd line fib, hypokalemia; LONG HALF LIFE
    - - B1 agonist ^ cAMP IV; increase calcium through L type
    - - affect renal causing vasodilation
      - B agonist producing cAMP ^
    - - phosphodiesterase inhibitor (cAMP) IV; vasodilator in increase B1 activity to the heart (EDV and SVR);